The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis

被引：54

作者：

Tao, Ye ^{[1
]}

Wang, Ningning ^{[2
]}

Qiu, Tianming ^{[1
]}

Sun, Xiance ^{[1
,3
]}

机构：

[1] Dalian Med Univ, Occupat & Environm Hlth Dept, 9 Lvshun South Rd, Dalian 116044, Peoples R China

[2] Dalian Med Univ, Nutr & Food Hyg, 9 Lvshun South Rd, Dalian 116044, Peoples R China

[3] Dalian Med Univ, Global Hlth Res Ctr, 9 Lvshun South Rd, Dalian 116044, Peoples R China

来源：

BIOMED RESEARCH INTERNATIONAL | 2020年 / 2020卷

基金：

中国国家自然科学基金;

关键词：

STELLATE CELL ACTIVATION; OXIDATIVE STRESS; PATHWAY; PYROPTOSIS; INHIBITOR; HYPOXIA; TARGETS; OXYGEN; BETA;

D O I：

10.1155/2020/7269150

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Liver fibrosis is an intrinsic repair process of chronic injury with excessive deposition of extracellular matrix. As an early stage of various liver diseases, liver fibrosis is a reversible pathological process. Therefore, if not being controlled in time, liver fibrosis will evolve into cirrhosis, liver failure, and liver cancer. It has been demonstrated that hepatic stellate cells (HSCs) play a crucial role in the formation of liver fibrosis. In particular, the activation of HSCs is a key step for liver fibrosis. Recent researches have suggested that autophagy and inflammasome have biological effect on HSC activation. Herein, we review current studies about the impact of autophagy and NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome on liver fibrosis and the underlying mechanisms.

引用

页数：8

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